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Carcinogenesis Advance Access published online on December 29, 2005
Carcinogenesis, doi:10.1093/carcin/bgi318
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received July 21, 2005
Revised September 17, 2005
Accepted December 17, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Suppression of colon carcinogenesis by bioactive compounds in grapefruit

Jairam Vanamala 1, Tety Leonardi 2, Bhimanagouda S. Patil 3, Stella S. Taddeo 2, Mary E. Murphy 4, Leonard M. Pike 3, Robert S. Chapkin 2, Joanne R. Lupton 2, and Nancy D. Turner 2 *

1 Department of Nutrition and Food Science, Texas A&M University, College Station, TX-77843; Vegetable and Fruit Improvement Center, Department of Horticultural Sciences, Texas A&M University, College Station, TX-77843
2 Department of Nutrition and Food Science, Texas A&M University, College Station, TX-77843
3 Vegetable and Fruit Improvement Center, Department of Horticultural Sciences, Texas A&M University, College Station, TX-77843
4 Department of Statistics, Texas A&M University, College Station, TX-77843

* To whom correspondence should be addressed.
Nancy D. Turner, E-mail: n-turner{at}tamu.edu


  Abstract

This study evaluated the hypothesis that untreated and irradiated grapefruit as well as the isolated citrus compounds naringin and limonin would protect against azoxymethane (AOM) induced aberrant crypt foci (ACF) by suppressing proliferation and elevating apoptosis through anti-inflammatory activities. Male Sprague Dawley rats (n = 100) were provided one of five diets: control (without added grapefruit components), untreated or irradiated (300 Gy, 137Cs) grapefruit pulp powder (13.7 g/kg), naringin (200 mg/kg) or limonin (200 mg/kg). Rats were injected with saline or AOM (15 mg/kg) during the 3rd and 4th wk and colons were resected (6 wk post 2nd injection) for evaluation of ACF, proliferation, apoptosis, and COX-2 and iNOS protein levels. Experimental diets had no effect on the variables measured in saline injected rats. However, in AOM-injected rats, the experimental diets suppressed (P ≤ 0.02) AC and high multiplicity ACF (P ≤ 0.01; HMACF) formation and the proliferative index (P ≤ 0.02) compared to the control diet. Only untreated grapefruit and limonin suppressed (P ≤ 0.04) HMACF/cm and expansion (P ≤ 0.008) of the proliferative zone that occurred in the AOM-injected rats consuming the control diet. All diets elevated (P ≤ 0.05) the apoptotic index in AOM-injected rats, compared to the control diet, however, the greatest enhancement was seen with untreated grapefruit and limonin. Untreated grapefruit and limonin diets suppressed elevation of both iNOS (P ≤ 0.003) and COX-2 (P ≤ 0.032) levels observed in AOM injected rats consuming the control diet. Although irradiated grapefruit and naringin suppressed iNOS levels in AOM injected rats, no effect was observed with respect to COX-2 levels. Thus, lower levels of iNOS and COX-2 are associated with suppression of proliferation and up-regulation of apoptosis, which may have contributed to a decrease in the number of HMACF in rats provided with untreated grapefruit and limonin. These results suggest that consumption of grapefruit or limonin may help to suppress colon cancer development.

Keywords: Grapefruit; Colon cancer; Cell turnover; iNOS; COX-2.
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